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Original Research: Pulmonary Vascular Disease |

Effect of Balloon Pulmonary Angioplasty on Respiratory Function in Patients With Chronic Thromboembolic Pulmonary Hypertension FREE TO VIEW

Mina Akizuki, PT; Naoki Serizawa, MD, PhD; Atsuko Ueno, MD, PhD; Taku Adachi, PT, MS; Nobuhisa Hagiwara, MD, PhD
Author and Funding Information

FUNDING/SUPPORT: The authors have reported to CHEST that no funding was received for this study.

aDepartment of Rehabilitation, Tokyo Women's Medical University, Tokyo, Japan

bDepartment of Cardiology, Tokyo Women's Medical University, Tokyo, Japan

cDepartment of Internal Medicine and Rehabilitation, Science Disability Science, Tohoku University Graduate School of Medicine, Sendai, Japan

CORRESPONDENCE TO: Mina Akizuki, PT, Department of Rehabilitation, Tokyo Women’s Medical University, 8-1 Kawadacho, Shinjuku-ku, Tokyo 162-0054, Japan


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2017;151(3):643-649. doi:10.1016/j.chest.2016.10.002
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Background  Balloon pulmonary angioplasty (BPA) in chronic thromboembolic pulmonary hypertension (CTEPH) improves hemodynamics and exercise capacity. However, its effect on respiratory function is unclear. Our objective was to investigate the effect of BPA on respiratory function.

Methods  We enrolled patients with inoperable CTEPH who underwent BPA primarily in lower lobe arteries (first series) and upper and middle lobe arteries (second series). We compared changes in hemodynamics and respiratory function between different BPA fields.

Results  Sixty-two BPA sessions were performed in 13 consecutive patients. Mean pulmonary arterial pressure and pulmonary vascular resistance significantly improved from 44 ± 8 to 23 ± 5 mm Hg and 818 ± 383 to 311 ± 117 dyne/s/cm−5. The percent predicted diffusion capacity of lung for carbon monoxide (Dlco) decreased after BPA in the lower lung field (from 60% ± 8% to 54% ± 8%) with no recovery. Percent Dlco increased after BPA in the upper middle lung field (from 53% ± 6% to 58% ± 6%) and continued to improve during the follow-up (from 58% ± 6% to 64% ± 11%). The ventilation/Co2 production (e/co2) slope significantly improved after BPA in the lower lung field (from 51 ± 13 to 41 ± 8) and continued to improve during the follow-up (from 41 ± 8 to 35 ± 7); however, the e/co2 slope remained unchanged after BPA in the upper/middle lung field. Changes in % Dlco and the e/co2 slope differed significantly between lower and upper/middle lung fields.

Conclusions  The effect of BPA on respiratory function in patients with CTEPH differed depending on the lung field.

Figures in this Article
Chronic thromboembolic pulmonary hypertension (CTEPH) has a poor prognosis because of increased pulmonary arterial pressure (PAP) causing pulmonary hypertension and progressive right-sided heart failure., Typical symptoms are dyspnea on exertion, fatigability (exercise tolerance), and reduced quality of life.,, Moreover, reduction of ventilation efficiency can occur in CTEPH because of increasing physiological dead space caused by hyperventilation and ventilation/perfusion (V˙ /Q˙ ) mismatch.,
Previously, balloon pulmonary angioplasty (BPA) has been reported to improve hemodynamics and functional capacity in patients with CTEPH who are not candidates for pulmonary endarterectomy., However, the effect of BPA on respiratory function is unclear. Adaptation of perfusion to ventilation is an important feature of pulmonary physiology; ventilation and pulmonary blood flow in different lung fields vary at rest and during exercise.,, BPA changes the V˙ /Q˙  ratio by improving pulmonary blood flow, and the effect of BPA on respiratory function may vary depending on the BPA fields, such as lower or upper/middle lung fields at rest and during exercise. In particular, carbon monoxide lung diffusion capacity (Dlco) reflects pulmonary capillary blood flow and V˙ /Q˙  mismatch.

We investigated how BPA affects hemodynamics, ventilatory efficiency, and gas exchange in patients with CTEPH using right heart catheterization, respiratory function testing, and cardiopulmonary exercise testing (CPX).

Patients

We enrolled consecutive patients with inoperable CTEPH who underwent BPA from May 2012 to December 2014. All patients were hospitalized twice.

BPA was performed primarily in lower lobe arteries during the first hospitalization (first series). After 3 months, patients were readmitted and underwent BPA in upper/middle lobe arteries (second series). In both series, BPA was repeated at a 1-week interval after the first and additional procedure and usually involved two to three sessions in each BPA series.

We divided the lung into two fields following definitions of pulmonary arteries and lung fields as outlined by Boyden: upper (A1-A3) and middle (A4-A5) lobe arteries were termed the upper/middle lung field, and lower lobe arteries (A6-A10) were termed the lower lung field.

We evaluated hemodynamics and respiratory functions before the first BPA session, within 1 week after final BPA, and 3 months after each final BPA series using the following methods. Right heart catheterization was performed the day after each final BPA series in all patients. We also measured the mean PAP (mPAP) at rest in the supine position, as well as pulmonary vascular resistance (PVR) and cardiac output (CO), which was measured by the Fick method.

Respiratory Function Tests

Respiratory function was evaluated using spirography, a flow-volume loop was performed on an electronic spirometry device (FUDAC-70; Fukuda Denshi Co.). To adjust for height, age, and sex we used prediction equations for FEV1 and FVC. We measured the Dlco by the single-breath method and calculated % Dlco. After a short period of tidal breathing, the patient exhaled maximally followed by inhalation to vital capacity of the test gas. The breath-holding time was recorded as the standard time (10 s).

Cardiopulmonary Exercise Testing
The CPX was performed on an upright cycle ergometer (Strength Ergo 8; Mitsubishi Electric Engineering). We performed the examination using a 5- to 10-W/min ramp load. After a 4-min rest on an ergometer, 4-min unloaded pedaling followed by increased exercise was performed. Patients were encouraged to perform a symptom-limited maximal test unless they met another indication for test termination (eg, dyspnea and leg fatigue). During the test, exercise test monitoring was performed using the Stress Test System (ML-9000; Fukuda Denshi Co.) with continuous heart rate and arrhythmia monitoring using 12-lead electrocardiography every minute. The 12-lead ECG was monitored continuously, and BP was measured every minute during exercise and throughout the recovery period. Pulse oximeters measuring oxyhemoglobin saturation (Spo2) were monitored continuously and results were recorded every minute. Respiratory gas exchange variables, including the oxygen consumption (V˙ o2), carbon dioxide output (V˙ co2), and minute V˙ e, were acquired continuously throughout the exercise test using Cpex-1 (Inter Reha Co.); gas exchange data were obtained using a breath-by-breath method. The V˙ e/V˙ co2 slope was determined using a linear regression analysis of V˙ e and V˙ co2 obtained during exercise. CPX parameters included peak V˙ o2 reflecting exercise capacity and disease severity, V˙ e/V˙ co2 slope, and end-tidal Co2 fraction (Fetco2) at the respiratory compensation point (RCP), the marker for V˙ /Q˙  ratio during exercise. To evaluate oxygenation under the same conditions between series and time course, we used the Spo2 at rest and a 40-W workload.
6-Min Walk Test

The 6-min walk test (6MWT) was performed according to standardized criteria. Patients were instructed to walk as far as possible for 6 min and were permitted to stop and rest if required. During the 6MWT, patients wore an electrocardiograph monitor and pulse oximeter (PULSOX300i; Konica Minolta Co.), which was connected to a portable pulse oximeter by a finger probe. Heart rate and Spo2 were recorded every minute. BP and the Borg score were measured before and after the 6MWT. Patients used supplemental oxygen when necessary and the same oxygen flow rate within the same series tests.

All patients provided informed consent to participate in the study. The study was carried out according to the principles of the Declaration of Helsinki, and the study protocol was approved by the institutional ethics committee (1796).

Statistical Analysis

Results are expressed as mean ± SD. Statistical analysis was performed using IBM SPSS Statistics, version 21 (SPSS Inc.). A two-sided P value of < .05 was considered statistically significant. Regarding the clinical course, a two-way analysis of variance with repeated measures was used to compare differences between series (lower lobe arteries vs upper and middle lobe arteries) and time course (before first BPA session, within 1 week after final BPA, and 3 months after each final BPA series), followed by Bonferroni’s post test (within-group analysis). The Mann-Whitney U test was used to compare pulmonary artery distribution and percent change in hemodynamics between each BPA series (between-group analysis).

We prospectively enrolled 13 consecutive patients with CTEPH who underwent two BPA series. In total, 62 BPA sessions were performed, and the average number of total BPA sessions per patient was 4.8 ± 0.6 (first series, 2.6 ± 0.7 sessions; second series, 2.2 ± 0.4 sessions). The baseline patient characteristics are shown in Table 1. Targeted artery percentages in each series are shown in Table 2. In the first BPA series, lower lobe arteries were targeted in most cases. There was no change in the amount of drug used during each BPA series before and after final BPA.

Table Graphic Jump Location
Table 1 Characteristics of Patients

6MWD = 6-min walk distance; CO = cardiac output; Dlco = diffusion capacity of lung for carbon monoxide; Fetco2 = end-tidal Co2 fraction; mPAP = mean pulmonary arterial pressure; PH = pulmonary hypertension; PVR = pulmonary vascular resistance; RCP = respiratory compensation point; V˙ e/V˙ co2 = ventilation to carbon dioxide production; V˙ o2 = oxygen consumption; WHO-FC, World Health Organization functional class.

Table Graphic Jump Location
Table 2 Distribution of Dilated Pulmonary Arteries in Each Series

Results are expressed as the number of arteries and the percentage of targeted arteries.

Hemodynamic Changes

We evaluated hemodynamics before and the day after the final BPA session and during follow-up (14 ± 5 weeks after final BPA) in each series. The mPAP and PVR improved after the final BPA session in lower and upper/middle lung fields, and improvement was maintained at follow-up (Table 3). CO tended to increase after the final BPA session in lower and upper/middle lung fields (P = .009 and P = .217, respectively); improvement was maintained at follow-up (Table 3).

Table Graphic Jump Location
Table 3 Hemodynamic Changes
a P < .01 vs pre-BPA.
b P < .05.

Results are expressed as mean ± SD.

BPA = balloon pulmonary angioplasty. See Table 1 legend for expansion of other abbreviations.

Comparison of the percent change in hemodynamics from baseline to after the final BPA session in the different fields showed the following: mPAP, −30% ± 12% vs −23% ± 19%; PVR, −39% ± 22% vs −23% ± 9%; CO, 33% ± 28% vs 17% ± 27% (lower lung field vs upper/middle lung field, respectively). Hemodynamic improvement tended to be larger for BPA in the lower lung field (Fig 1).

Figure 1
Figure Jump LinkFigure 1 Comparison of the percent change in hemodynamic results from baseline to after final balloon pulmonary angioplasty primarily in lower lobe arteries (first series) and upper/middle lobe arteries (second series). mPAP = mean pulmonary arterial pressure; NS = not significant; PVR = pulmonary vascular resistance.Grahic Jump Location
Spo2 Changes at Rest and During Exercise Change

Spo2 at rest improved after the final BPA session in the lower lung field (from 92.7% ± 3.3% to 94.8% ± 2.7%; P = .020), which was maintained at follow-up. The upper/middle lung field showed no significant difference in Spo2 at rest after the final BPA session (from 95.1% ± 1.4% to 96.5% ± 1.4%; P = .636). However, Spo2 increased steadily during the follow-up. At a 40-W workload, Spo2 tended to improve after the final BPA session in the lower lung field (from 87.6% ± 4.3% to 89.2% ± 3.4%; P = .251), which was maintained during follow-up. After BPA in the upper/middle lung field, Spo2 at a 40-W workload significantly improved (from 89.4% ± 2.6% to 93.4% ± 2.9%; P = .043) and continued to improve during the follow-up.

Respiratory Function Change

Percent Dlco significantly decreased after the final BPA session in the lower lung field (from 60% ± 8% to 54% ± 8%; P = .001) and did not appear to recover during the follow-up period. In contrast, % Dlco significantly increased after the final BPA session in the upper/middle lung field (from 53% ± 6% to 58% ± 6%; P = .030) and continued to increase during the follow-up (from 58% ± 6% to 64% ± 11%; P = .077) (Fig 2). Furthermore, the time course of the change in % Dlco varied significantly depending on the BPA field (P < .001).

Figure 2
Figure Jump LinkFigure 2 Time course of changes in carbon monoxide lung diffusion capacity after balloon pulmonary angioplasty. P values represent the interaction between balloon pulmonary angioplasty fields and time course as within-subjects effects. BPA = balloon pulmonary angioplasty; Dlco = diffusion capacity of lung for carbon monoxide.Grahic Jump Location
The V˙ e/V˙ co2 slope improved after the final BPA session in the lower lung field (from 51 ± 13 to 41 ± 8; P = .014) and showed further improvement from after the final BPA session to the follow-up (from 41 ± 8 to 35 ± 7; P = .007). In contrast, the V˙ e/V˙ co2 slope was unchanged after the final BPA session in the upper/middle lung field (from 35 ± 7 to 37 ± 6; P = 1.000). Fetco2 improved after the final BPA session in the lower lung field (from 3.93 ± 0.36 to 4.40 ± 0.59; P < .001) and showed further improvement after the final BPA session to the follow-up (from 4.40 ± 0.59 to 4.85 ± 0.40; P = .003). In contrast, Fetco2 was unchanged after the final BPA session in the upper/middle lung field (from 4.85 ± 0.48 to 4.83 ± 0.43; P = .782) and tended to recover to the same levels as before the first BPA session (from 4.83 ± 0.43 to 4.96 ± 0.53; P = .084) (Fig 3). The time course of changes in the V˙ e/V˙ co2 slope and Fetco2 were significantly different between lower and upper/middle lung BPA fields (P = .020 and P = .007, respectively).
Figure 3
Figure Jump LinkFigure 3 Time course of changes in cardiopulmonary exercise test parameters after balloon pulmonary angioplasty. A, V˙ e/V˙ co2 slope. B, Fetco2. P values represent the interaction between balloon angioplasty fields and time course as within-subjects effects. Fetco2, end-tidal Co2 fraction; V˙ e/V˙ co2 = ventilation/Co2 production.Grahic Jump Location
This is the first study showing differences in the effect of BPA on respiratory function in different BPA fields in patients with CTEPH. Oxygenation at rest and during exercise improved regardless of the BPA field. However, the time course of changes in % Dlco, V˙ e/V˙ co2 slope, and Fetco2 was significantly different between lower and upper/middle lung BPA fields.
Change of % Dlco
Percent Dlco decreased after the final BPA session in the lower lung field and did not appear to recover during follow-up (first series). In contrast, % Dlco increased after the final BPA session in the upper/middle lung field and continued increasing during the follow-up (second series) (Fig 2). Furthermore, the time course of the change in % Dlco was significantly different between lower and upper/middle lung BPA fields. This is probably related to the change in the V˙ /Q˙  ratio.
From the Foster equation, Dlco is represented by the following formula:where DM is the pulmonary membrane diffusion capacity and VC is the pulmonary capillary blood volume (VC). However, the diffusion capacity differs depending on position., The diffusion area in respiratory function tests is different from the anatomic diffusion area and is determined by the functional blood flow in contact with functional alveoli. In VC, V˙ /Q˙  mismatch can more strongly affect Dlco than pulmonary blood flow volume. Thus, V˙ /Q˙  mismatch is caused by the gravitational effect even in normal lungs. The lower lung field experiences more perfusion than ventilation (low V˙ /Q˙  unit); the upper lung field experiences more ventilation than perfusion (high V˙ /Q˙  unit). In this study, BPA improved pulmonary blood flow. It created more low V˙ /Q˙  units and increased V˙ /Q˙  mismatch in the lower lung field. However, the upper/middle lung field had high V˙ /Q˙  units. Therefore, BPA improved the V˙ /Q˙  mismatch. An increase in total pulmonary blood flow causes even more V˙ /Q˙  mismatch exacerbation by diverting more perfusion to the already lower V˙ /Q˙  units. For this reason, BPA produced different V˙ /Q˙  patterns between lower and upper/middle lung BPA fields, and a change in % Dlco varies depending on the BPA fields.
Changes in the V˙e/V˙co2 Slope and Fetco2
The V˙ e/V˙ co2 slope indicates ventilation efficiency during exercise. In CTEPH, the V˙ e/V˙ co2 slope is high because of reduced ventilation efficiency; an increase in dead space is caused by thromboembolic obstruction and V˙ /Q˙  mismatch. In the present study, the V˙ e/V˙ co2 slope improved significantly after the final BPA session in the lower lung field and showed further improvement from the final BPA session to the follow-up. In contrast, the V˙ e/V˙ co2 slope remained unchanged after the final BPA session in the upper/middle lung field. Furthermore, the time course of the change in the V˙ e/V˙ co2 slope was significantly different between lower and upper/middle lung BPA fields (Fig 3).
Physiologically, there is a greater blood flow distribution in the lower than in the upper/middle lung field. Improvements in CO and PVR correlated with a decrease in the V˙ e/V˙ co2 slope., In the present study, improvement in CO and PVR after the final BPA session was higher in the lower lung field than in the upper/middle lung field (Fig 1), and the V˙ e/V˙ co2 slope significantly improved in the lower lung field but not in the upper/middle lung field (Fig 3).
PETCo2 at the RCP correlated negatively with the ratio of physiological dead space to tidal volume. Fetco2 is reduced in patients with CTEPH because of increased physiological dead space due to a V˙ /Q˙  mismatch caused by restriction of the increase in pulmonary blood flow during exercise. Therefore, Fetco2 at the RCP reflects the V˙ /Q˙  ratio during exercise. In the present study, Fetco2 significantly improved after the final BPA session and the follow-up in the lower lung field, whereas it did not change after the final BPA session in the upper/middle lung field in either evaluation period. Normally, exercise leads to increased V˙ e and improves V˙ /Q˙  mismatch. BPA in the lower lung field might improve the V˙ /Q˙  mismatch during exercise because of improvement in CO and increased V˙ e. However, BPA in the upper/middle lung field produced a small improvement in CO and had little effect on V˙ /Q˙  mismatch during exercise. For this reason, Fetco2 significantly improved in the lower lung field but not in the upper/middle lung field (Fig 3).
Based on our results, we suggest that BPA in the lower lung field improves oxygenation and respiratory function parameters during exercise, such as V˙ e/V˙ co2 slope and Fetco2, because of remarkable improvement in hemodynamics. BPA in the upper/middle lung field may improve oxygenation and respiratory function parameters at rest, such as % Dlco, caused by improvement in V˙ /Q˙  mismatch.
Limitations

Our study had several limitations. The observation period was not long, and the number of patients was small. Additionally, BPA was performed primarily in lower lobe arteries (first series). BPA was then performed in the upper/middle lobe arteries (second series) after some improvement was obtained following BPA in the lower lobe. Moreover, patients were treated with drugs targeted for pulmonary hypertension. Therefore, it is possible that the effect of time and drug effects on respiratory function cannot be excluded.

During follow-up, changes in % Dlco and the V˙ e/V˙ co2 slope were significantly different between lower and upper/middle lung BPA fields. The results suggest that the effect of BPA on respiratory function in patients with CTEPH varies depending on the BPA fields.

Author contributions: M. A. is the guarantor of this article. M. A. and N. S. contributed to the conception and design of the study, analysis and interpretation of data, and writing of the manuscript. A. U. and T. A. conducted the study. N. H. revised the manuscript.

Financial/nonfinancial disclosures: None declared.

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Figures

Figure Jump LinkFigure 1 Comparison of the percent change in hemodynamic results from baseline to after final balloon pulmonary angioplasty primarily in lower lobe arteries (first series) and upper/middle lobe arteries (second series). mPAP = mean pulmonary arterial pressure; NS = not significant; PVR = pulmonary vascular resistance.Grahic Jump Location
Figure Jump LinkFigure 2 Time course of changes in carbon monoxide lung diffusion capacity after balloon pulmonary angioplasty. P values represent the interaction between balloon pulmonary angioplasty fields and time course as within-subjects effects. BPA = balloon pulmonary angioplasty; Dlco = diffusion capacity of lung for carbon monoxide.Grahic Jump Location
Figure Jump LinkFigure 3 Time course of changes in cardiopulmonary exercise test parameters after balloon pulmonary angioplasty. A, V˙ e/V˙ co2 slope. B, Fetco2. P values represent the interaction between balloon angioplasty fields and time course as within-subjects effects. Fetco2, end-tidal Co2 fraction; V˙ e/V˙ co2 = ventilation/Co2 production.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1 Characteristics of Patients

6MWD = 6-min walk distance; CO = cardiac output; Dlco = diffusion capacity of lung for carbon monoxide; Fetco2 = end-tidal Co2 fraction; mPAP = mean pulmonary arterial pressure; PH = pulmonary hypertension; PVR = pulmonary vascular resistance; RCP = respiratory compensation point; V˙ e/V˙ co2 = ventilation to carbon dioxide production; V˙ o2 = oxygen consumption; WHO-FC, World Health Organization functional class.

Table Graphic Jump Location
Table 2 Distribution of Dilated Pulmonary Arteries in Each Series

Results are expressed as the number of arteries and the percentage of targeted arteries.

Table Graphic Jump Location
Table 3 Hemodynamic Changes
a P < .01 vs pre-BPA.
b P < .05.

Results are expressed as mean ± SD.

BPA = balloon pulmonary angioplasty. See Table 1 legend for expansion of other abbreviations.

References

Hoeper M.M. .Mayer E. .Simonneau G. .Rubin L.J. . Chronic thromboembolic pulmonary hypertension. Circulation. 2006;113:2011-2020 [PubMed]journal. [CrossRef] [PubMed]
 
Jenkins D. .Mayer E. .Screaton N. .Madani M. . State-of-the-art chronic thromboembolic pulmonary hypertension diagnosis and management. Eur Respir Rev. 2012;21:32-39 [PubMed]journal. [CrossRef] [PubMed]
 
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    Print ISSN: 0012-3692
    Online ISSN: 1931-3543